Research was performed on a group of 30 patients with non-insulin-dependent diabetes mellitus (NIDDM), who never received antidiabetic medication before, and on a group of 17 healthy adults. The patients were administered treatment with metformin, 1,000 mg/day. Plasmatic and urinary concentration of magnesium have been measured, copper and zinc along with the concentrations of glucose, HDL, LDL, cholesterol, tryglicerides, HbA1c, and total erythrocyte magnesium, in advance and after 3 months of treatment. Data showed significant differences in the NIDDM group vs the control group: for plasma magnesium-1.95 ± 0.19 vs 2.20 ± 0.18 mg/dl, p < 0.001; urine magnesium-237.28 ± 34.51 vs 126.25 ± 38.22 mg/24 h, p < 0.001; erythrocyte magnesium-5.09 ± 0.63 vs 6.38 ± 0.75 mg/dl, p < 0.001; plasma zinc-67.56 ± 6.21 vs 98.41 ± 20.47 μg/dl, p < 0.001; urine zinc-1,347.54 ± 158.24 vs 851.65 ± 209.75 μg/24 h, p < 0.001; plasma copper-111.91 ± 20.98 vs 96.33 ± 8.56 μg/dl, p < 0.001; and urine copper-51.70 ± 23.79 vs 36.00 ± 11.70 μg/24 h, p < 0.05. Treatment with metformin for 3 months modified significant erythrocyte magnesium-5.75 ± 0.61 vs 5.09 ± 0.63 mg/dl, p < 0.001 and urine magnesium-198.27 ± 27.07 vs 237.28 ± 34.51 mg/24 h, p < 0.001, whereas it did not modify significant the plasmatic and urinary concentration of the other cations. The erythrocyte magnesium concentration was inversely correlated with HbA1c (r = -0.438, p = 0.015). The plasma level of copper was positively correlated with HbA1c (r = 0.517, p < 0.003), tryglicerides (r = 0.534, p < 0.003), and cholesterol (r = 0.440, p < 0.05), and the plasma level of zinc was inversely correlated with glycemia (r = -0.399, p = 0.029). Our data show a significant action of metformin therapy, by increasing the total intraerythrocyte magnesium concentration and decreasing the urinary magnesium elimination, positively correlated with the decrease of glycemia and HbA1c in NIDDM patients.

Kaposi’s sarcoma is a rare disease with four known variants: classic, epidemic, endemic and iatrogenic (transplant-related), all caused by an oncogenic virus named Human Herpes Virus 8. The viral infection in itself, along with the oncogenic properties of HHV8 and with immune system dysfunction, forms the grounds on which Kaposi’s Sarcoma may develop. Infection with HHV8 occurs through saliva via close contacts, blood, blood products, solid organ donation and, rarely, vertical transmission. Chronic inflammation and oncogenesis are promoted by a mix of viral genes that directly promote cell survival and transformation or interfere with the regular cell cycle and cell signaling (of particular note: LANA-1, v-IL6, vBCL-2, vIAP, vIRF3, vGPCR, gB, K1, K8.1, K15). The most common development sites for Kaposi’s sarcoma are the skin, mucocutaneous zones, lymph nodes and visceral organs, but it can also rarely appear in the musculoskeletal system, urinary system, endocrine organs, heart or eye. Histopathologically, spindle cell proliferation with slit-like vascular spaces, plasma cell and lymphocyte infiltrate are characteristic. The clinical presentation is heterogenic depending on the variant; some patients have indolent disease and others have aggressive disease. The treatment options include highly active antiretroviral therapy, surgery, radiation therapy, chemotherapy, and immunotherapy. A literature search was carried out using the MEDLINE/PubMed, SCOPUS and Google Scholar databases with a combination of keywords with the aim to provide critical, concise, and comprehensive insights into advances in the pathogenic mechanism of Kaposi’s sarcoma.

No abstract

Experimental studies and clinical trials revealed the complex interconnections between imidazoline system and various other mediators such as epinephrine, norepinephrine; thus, explain their involvement in the pathophysiological mechanisms of different motor, behavioral and cognitive disturbances. In this study, we tested the influence induced by idazoxan and efaroxan on the cognitive performances in rats. Groups of 6 adult male Wistar rats were treated intraperitoneally according to the following protocol: group I (Control): distilled water 0.3 ml/100g; group II (IDZ): 3 mg/kg idazoxan and group III (EFR): 1 mg/kg efaroxan. The effects of the imidazoline receptor antagonists on the rats cognitive functions were assessed using the radial-arm maze, in order to count the time spent into the arms, the number of baited arms visited, but previously explored (working memory errors); the time taken to consume all baits and the number of entering in non-baited arms (reference memory errors). The data were expressed as mean +/- standard deviation, and statistically analyzed using SPSS version 17.0 Software for Windows, followed by ANOVA one-way method. The administration of IDZ, as well as of EFR was accompanied by a substantial diminution in the number of working memory errors, and the period of time to consume all baits, statistically significant (p[0.01) compared to control group. The use of these two imidazoline receptors antagonists resulted in a considerable decrease in the reference memory errors number, statistically significant (p[0.01) compared to the group treated with distilled water. The influence of IDZ on the evaluated parameters was more accentuated than the effects induced by EFR in all sessions of testing, in this behavioral experimental model. Our findings indicate that treatment with both imidazoline receptor antagonists, idazoxan and efaroxan was associated by a facilitation of the short-term memory retention, an enhancement of discriminative spatial learning, and an improvement of long-term memory performance in radial arm maze in rats.

The connection between oxidative stress and ocular injuries was highly debated, given the fact that, as a result of its particular structure, the eye may have different reactions when exposed to oxidative stress and visual activity and functionality are considerable compromised. Our experimental research focused on two types of induced oxidative stress on rats (disruption of circadian rhythm and diabetes mellitus) with impact on biochemical markers of oxidative stress. We have analysed the amplitude of significant antioxidant markers correlated with each individual type of antioxidant disorder. We observed alterations of stress biomarkers for all induced types of stress, but the most relevant are associated with diabetes mellitus and light exposure.